Previous research on the early onset of puberty has focused on specific subpopulations or clinical populations, and data on the patterns of pubertal onset, that is, in children as young as ages 6 to 8 years, in a nationally representative sample are lacking. A need exists for determining if there has been a decline in the age of pubertal onset nationally, especially in light of two concerns: (1) the intertwining of early pubertal onset with national trends toward increased child overweight and obesity, and (2) suggestions that the age limit for defining precocious puberty, as compared with normal early puberty, should be lowered to accommodate the suspected secular decline. Further, evidence suggests that exposure to environmental toxins, such as environmental lead (Pb) and endocrine disrupters, may adversely affect hormone levels and pubertal onset. However, data on how and whether environmental toxicants may be implicated in the decline or contribute to a delay in pubertal onset are scarce and have generally been confined to older children and adolescents.[unreadable] [unreadable] There are two objectives of these analyses of stored biologic specimens (serum) for children, ages 6-11 years examined as part of the Third National Health and Nutrition Examination Survey (NHANES III), 1988-94: (1) to estimate by assay of hormones (luteinizing hormone [LH] and inhibin B for boys and girls, testosterone for boys) the timing of the onset of pubertal development in a nationally representative sample of children, ages 6-11 years, and the concordance between hormonal indicators and pubertal onset based on physical maturation (Tanner sexual maturation scores) for children, ages 8-11 years; and (2) to determine if the recent findings linking blood lead (Pb) levels and delayed maturation based on Tanner scores (pubic hair) and age at menarche in girls can be confirmed by hormonal analysis and extended to younger ages and to determine for young boys if there are effects of blood Pb levels on timing of maturation. To address study objectives, the target sample for these analyses is children, ages 6-11 years, examined as part of the Third National Health and Nutrition Examination Survey, 1988-94. Because limited amounts of stored sera are available for children in the 6-11 year age range, the two main hormones selected for analysis to detect the onset of puberty were chosen to provide the maximum sensitivity (using a minimum of serum sample, 0.2 mL) and can be analyzed for both boys and girls. In order of priority, we will measure luteinizing hormone (LH) and inhibin B. On those samples with insufficient quantity to do both, inhibin B will be measured for boys and LH for girls. On a subset of boys who have adequate stored sample, testosterone will be measured. In terms of correlates of pubertal onset, NHANES III data are already available in public domain, including socio-demographic and anthropometric measurements, as well as Tanner scores collected at ages 8-11, for validation of the hormonal indicators at those ages. Because Tanner scores or other measures of pubertal onset have not been collected as part of subsequent NHANES surveys, if the hormones are found to be sensitive indicators of the onset of pubertal development, this study could form the basis and justification for extending the hormone analyses to earlier (NHANES I and II) and later NHANES (1999-2000, 2001-2002, 2003-2004) samples to determine the extent of secular trends in the timing of pubertal onset at a national level.[unreadable] [unreadable] To meet the second objective, whole blood Pb and, in addition, urinary cadmium (Cd) have already been analyzed for examined children in NHANES III. It is important to note that the 6-11 year old children in NHANES III were born in the years 1977-1988, before the Lead Contamination Control Act of 1988 virtually eliminated Pb in gasoline, so it is unlikely that later iterations of NHANES will be as useful in answering the question about the relationship between environmental Pb exposure and timing of puberty.